NeuroMolecular Medicine最新文献_第9页

Altered Expression of miR-575 in Glioma is Related to Tumor Cell Proliferation, Migration, and Invasion. miR-575在胶质瘤中的表达改变与肿瘤细胞的增殖、迁移和侵袭有关。

IF 3.5 4区医学

NeuroMolecular Medicine Pub Date : 2022-06-01 Epub Date: 2021-07-16 DOI: 10.1007/s12017-021-08679-7

Guangxin Wei, Shengjun Li, Pengcheng Wang, Shouxian Wang, Yujing Zhao

{"title":"Altered Expression of miR-575 in Glioma is Related to Tumor Cell Proliferation, Migration, and Invasion.","authors":"Guangxin Wei, Shengjun Li, Pengcheng Wang, Shouxian Wang, Yujing Zhao","doi":"10.1007/s12017-021-08679-7","DOIUrl":"https://doi.org/10.1007/s12017-021-08679-7","url":null,"abstract":"Glioma is a kind of brain tumor with low overall survival and treatment success rates in the advanced stage. Evidence has shown microRNA-575 (miR-575) plays an important role in the generation and development of various cancers. This study aimed to explore the function of miR-575 in the prognosis and cell biological behavior of glioma. qRT-PCR was used to evaluate the expression of miR-575 in glioma tissues and cells, Kaplan-Meier survival analysis and Cox regression analysis were used to evaluate the prognostic value. The proliferation ability of glioma cells was determined by MTT assay; the invasion and migration abilities were determined by transwell assays. Compared with normal brain tissues, the expression of miR-575 in glioma tissue cells was significantly up-regulated (P < 0.001). The survival rate of patients in the miR-575 high expression group was significantly lower than that in the low expression group (P = 0.020). In addition, the overexpression of miR-575 promoted the proliferation, migration, and invasion of glioma cells. The results of this study suggested that miR-575 may be a new biomarker for the prognosis of glioma.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12017-021-08679-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39195526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Receptor-Interacting Protein 140 Enhanced Temozolomide-Induced Cellular Apoptosis Through Regulation of E2F1 in Human Glioma Cell Lines. 受体相互作用蛋白140通过调节人脑胶质瘤细胞系E2F1增强替莫唑胺诱导的细胞凋亡。

IF 3.5 4区医学

NeuroMolecular Medicine Pub Date : 2022-06-01 Epub Date: 2021-06-01 DOI: 10.1007/s12017-021-08667-x

Hong-Chieh Tsai, Kuo-Chen Wei, Pin-Yuan Chen, Chiung-Yin Huang, Ko-Ting Chen, Ya-Jui Lin, Hsiao-Wei Cheng, Chun-Hao Huang, Hsiang-Tsui Wang

{"title":"Receptor-Interacting Protein 140 Enhanced Temozolomide-Induced Cellular Apoptosis Through Regulation of E2F1 in Human Glioma Cell Lines.","authors":"Hong-Chieh Tsai, Kuo-Chen Wei, Pin-Yuan Chen, Chiung-Yin Huang, Ko-Ting Chen, Ya-Jui Lin, Hsiao-Wei Cheng, Chun-Hao Huang, Hsiang-Tsui Wang","doi":"10.1007/s12017-021-08667-x","DOIUrl":"https://doi.org/10.1007/s12017-021-08667-x","url":null,"abstract":"Glioblastoma (GBM), a grade IV glioma, is responsible for the highest years of potential life lost among cancers. The poor prognosis is attributable to its high recurrence rate, caused in part by the development of resistance to chemotherapy. Receptor-interacting protein 140 (RIP140) is a very versatile coregulator of nuclear receptors and transcription factors. Although many of the pathways regulated by RIP140 contribute significantly to cancer progression, the function of RIP140 in GBM remains to be determined. In this study, we found that higher RIP140 expression was associated with prolonged survival in patients with newly diagnosed GBM. Intracellular RIP140 levels were increased after E2F1 activation following temozolomide (TMZ) treatment, which in turn modulated the expression of E2F1-targeted apoptosis-related genes. Overexpression of RIP140 reduced glioma cell proliferation and migration, induced cellular apoptosis, and sensitized GBM cells to TMZ. Conversely, knockdown of RIP140 increased TMZ resistance. Taken together, our results suggest that RIP140 prolongs the survival of patients with GBM both by inhibiting tumor cell proliferation and migration and by increasing cellular sensitivity to chemotherapy. This study helps improve our understanding of glioma recurrence and may facilitate the development of more effective treatments.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12017-021-08667-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39051533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Influence of Simulated Deep Brain Stimulation on the Expression of Inflammatory Mediators by Human Central Nervous System Cells In Vitro. 模拟脑深部刺激对体外人中枢神经系统细胞炎症介质表达的影响。

IF 3.5 4区医学

NeuroMolecular Medicine Pub Date : 2022-06-01 Epub Date: 2021-07-03 DOI: 10.1007/s12017-021-08674-y

Carolin Kubelt, Henri Molkewehrum, Ralph Lucius, Michael Synowitz, Janka Held-Feindt, Ann-Kristin Helmers

{"title":"Influence of Simulated Deep Brain Stimulation on the Expression of Inflammatory Mediators by Human Central Nervous System Cells In Vitro.","authors":"Carolin Kubelt, Henri Molkewehrum, Ralph Lucius, Michael Synowitz, Janka Held-Feindt, Ann-Kristin Helmers","doi":"10.1007/s12017-021-08674-y","DOIUrl":"https://doi.org/10.1007/s12017-021-08674-y","url":null,"abstract":"Deep brain stimulation (DBS) seems to modulate inflammatory processes. Whether this modulation leads to an induction or suppression of inflammatory mediators is still controversially discussed. Most studies of the influence of electrical stimulation on inflammation were conducted in rodent models with direct current stimulation and/or long impulses, both of which differ from the pattern in DBS. This makes comparisons with the clinical condition difficult. We established an in-vitro model that simulated clinical stimulation patterns to investigate the influence of electrical stimulation on proliferation and survival of human astroglial cells, microglia, and differentiated neurons. We also examined its influence on the expression of the inflammatory mediators C-X-C motif chemokine (CXCL)12, CXCL16, CC-chemokin-ligand-2 (CCL)2, CCL20, and interleukin (IL)-1β and IL-6 by these cells using quantitative polymerase chain reaction. In addition, protein expression was assessed by immunofluorescence double staining. In our model, electrical stimulation did not affect proliferation or survival of the examined cell lines. There was a significant upregulation of CXCL12 in the astrocyte cell line SVGA, and of IL-1β in differentiated SH-SY5Y neuronal cells at both messenger RNA and protein levels. Our model allowed a valid examination of chemokines and cytokines associated with inflammation in human brain cells. With it, we detected the induction of inflammatory mediators by electrical stimulation in astrocytes and neurons.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12017-021-08674-y","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39077606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Tranilast, a Transient Receptor Potential Vanilloid 2 Channel (TRPV2) Inhibitor Attenuates Amyloid β-Induced Cognitive Impairment: Possible Mechanisms. 瞬时受体电位香草蛋白2通道(TRPV2)抑制剂曲尼司特减轻淀粉样蛋白β诱导的认知障碍:可能的机制。

IF 3.5 4区医学

NeuroMolecular Medicine Pub Date : 2022-06-01 Epub Date: 2021-07-06 DOI: 10.1007/s12017-021-08675-x

Pavan Thapak, Mahendra Bishnoi, Shyam Sunder Sharma

{"title":"Tranilast, a Transient Receptor Potential Vanilloid 2 Channel (TRPV2) Inhibitor Attenuates Amyloid β-Induced Cognitive Impairment: Possible Mechanisms.","authors":"Pavan Thapak, Mahendra Bishnoi, Shyam Sunder Sharma","doi":"10.1007/s12017-021-08675-x","DOIUrl":"https://doi.org/10.1007/s12017-021-08675-x","url":null,"abstract":"Alzheimer's disease (AD) is associated with the accumulation of β-amyloid and leads to cognitive impairment. Numerous studies have established that neuronal calcium homeostasis is perturbed in AD. Recently, transient receptor potential vanilloid 2 (TRPV2) channels, a non-selective calcium-permeable channel, have been investigated in several diseases. However, the role of the TRPV2 channel has not been investigated in AD yet. In this study, intracerebroventricular administration of β-amyloid (10 μg) to Sprague Dawley rats resulted in cognitive impairment which was evident from the assessment of cognitive tests. Also, TRPV2 mRNA and protein expression were found to be upregulated, while the expression of Ca2+/calmodulin-dependent protein kinase II (p-CaMKII-Thr-286), glycogen synthase kinase 3β (p-GSK-3β-Ser-9), cAMP response element-binding protein (p-CREB-Ser-133), and postsynaptic density protein 95 (PSD-95) were downregulated in the hippocampus of β-amyloid-treated animals. Even, β-amyloid-treated animals showed upregulation of mRNA level of calcium buffering proteins (parvalbumin and calsequestrin) and calcineurin A (PPP3CA) in the hippocampus. Acetylcholinesterase activity was also increased in the cortex of β-amyloid-treated animals. Three-week treatment with tranilast showed improvement in the cognitive parameters which was associated with a decrease in TRPV2 expression and AChE activity. Additionally, an increase in the protein expression of p-CaMKII, p-GSK-3β, p-CREB and PSD-95 in the hippocampus was found. Downregulation in the mRNA level of calcium buffering proteins (parvalbumin and calsequestrin) and calcineurin A in the hippocampus was also seen. These results reveal the importance of TRPV2 channels in the β-amyloid-induced cognitive deficits and suggest TRPV2 as a potential target for AD.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12017-021-08675-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39159845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 13

Neural Stem Cells Secretome Increased Neurogenesis and Behavioral Performance and the Activation of Wnt/β-Catenin Signaling Pathway in Mouse Model of Alzheimer’s Disease 阿尔茨海默病小鼠模型中神经干细胞分泌增加神经发生和行为表现及Wnt/β-儿茶素信号通路的激活

IF 3.5 4区医学

NeuroMolecular Medicine Pub Date : 2022-05-16 DOI: 10.1007/s12017-022-08708-z

Farzaneh Hijroudi, R. Rahbarghazi, S. Sadigh-Eteghad, G. Bahlakeh, M. Hassanpour, M. Shimia, Mohammad Karimipour